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S100A4 facilita la repoblación del tumor inducida por la radiación impulsando el brote de las células cancerosas
Ruyi Zhao1, Yanwei Song2, Jianzhu Xie2
1Department of Vascular Surgery, Shanghai General Hospital of Nanjing Medical University, Shanghai, China.
Cancer letters
|September 6, 2025
Resumen
Las células cancerosas gigantes poliploides (PGCC) impulsan la repoblación del cáncer colorrectal después de la radioterapia. Dirigirse a la vía S100A4-ISG15 inhibe el brote de PGCC, superando la resistencia al tratamiento y mejorando la sensibilidad a la radiación.
Área de la Ciencia:
- En el campo de la oncología
- Biología del cáncer
- Investigación en radioterapia
Sus antecedentes:
- La radioterapia es crucial para el tratamiento del cáncer colorrectal (CRC), pero a menudo está limitada por la repoblación del tumor.
- Las células cancerosas gigantes poliploides (PGCC) emergen después de la radiación, impulsando la resistencia y la repoblación a través de un proceso de brote único.
- La regulación molecular del brote de PGCC y su evasión de las salvaguardas de proliferación no se comprenden completamente.
Objetivo del estudio:
- Para aclarar los mecanismos moleculares que rigen el ciclo de vida de PGCC y el inicio de la radioterapia en CRC.
- Identificar los reguladores clave del brote de PGCC y su papel en la resistencia terapéutica.
- Explorar posibles objetivos terapéuticos para superar el fracaso de la radioterapia.
Principales métodos:
- Se emplearon transcriptómica de una sola célula y genómica funcional.
- Se utilizaron modelos longitudinales para rastrear la dinámica de PGCC.
- Investigó el papel de S100A4, RAGE y la señalización de interferón en el brote de PGCC.
Principales resultados:
- S100A4 está regulado en PGCC después de la radioterapia y es crucial para su capacidad de brote.
- S100A4 funciona a través del receptor RAGE y suprime la señalización de interferón I mediada por IRF3, aliviando la inhibición del brote mediada por ISG15/BST2.
- La inhibición de RAGE o S100A4 dificulta el brote de PGCC y restaura la radiosensibilidad.
Conclusiones:
- El eje S100A4-ISG15 es un regulador clave de la resistencia a la radioterapia en el CCR.
- La expresión S100A4-ISG15 o una " puntuación de brote viral " pueden predecir la respuesta al tratamiento.
- La orientación hacia el eje S100A4-ISG15 ofrece una estrategia potencial para superar la persistencia adaptativa en la CRC.
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